1. Field of the Invention
The invention of this application pertains to a vaccine for channel catfish virus, and in particular, a recombinant vaccine with gene 50 of the wild type or V60 channel catfish virus deleted or substantially deleted from the channel catfish virus. This invention also pertains to methods of vaccinating channel catfish against channel catfish virus, using the gene 50-deleted recombinant virus.
2. Background of the Prior Art
Channel catfish virus (CCV) (Ictalurid herpesvirus-1) is a cytopathic herpesvirus that can cause an acute, hemorrhagic, and lethal disease in the channel catfish Ictalurus punctatus (Fijan, 1968). Acute CCV epizootics in populations of fry and fingerling channel catfish can result in mortalities as high as 95% within one week (Plumb, 1978).
To date, three kinds of vaccines against CCV have been described in the literature. The first used a classically attenuated strain of the CCV Auburn strain (strain V60, Hartmann and Noga, 1980; Noga and Hartmann, 1981); the second was a subunit vaccine based on a preparation of viral envelope proteins (Awad et al. 1987); the third uses a live, thymidine-kinase-negative recombinant (Zhang and Hanson, 1995).
Considering the increasing importance of the channel catfish as a food source, the desirability of obtaining a vaccine for CCV to prevent the economic loss in hatcheries is evident. We studied the attenuated V60 strain, produced by multiple passages in cultured alternate host cells. The strain provides a protective vaccine strain against wild-type virus. When administered parenterally or as a water-borne vaccine, the strain was found to protect catfish fingerlings against a viral challenge, promoting a survival rate of over 90% (Walczak et al., 1981). A major deletion was found in gene 50 of the V60 strain (Vanderhejiden et al, 1996). Gene 50 encodes a secreted glycoprotein, highly glycosylated like the mucin-type glycoproteins, designated gp 250 (Vanderheijden, et al., 1999). Few viral glycoproteins are secreted upon herpesvirus infection (Randall et al 1980) and their function in the viral cycle by is still unclear. Since the attenuated V60 strain possesses a large deletion in its gene 50, the possibility exists that this gene could be responsible, at least in part, for the virulence of the wild-type strain. This possibility, therefore, offers a potential vaccine development route.